Innate immunity, through late complement components activation, contributes to the development of early vascular inflammation and morphologic alterations in experimental diabetes

F. Fischetti, R. Candido, B. Toffoli, P. Durigutto, S. Bernardi, R. Carretta, F. Tedesco, B. Fabris

Research output: Contribution to journalArticle

Abstract

Objective: To verify if innate immunity, and namely the assembly of terminal complement complex (TCC) could be involved in the development of early diabetic vascular damage. Methods and results: At first in 2 groups of diabetic or non-diabetic Wistar rats the occurrence of basal or stimulated stable adherence to the endothelial layer and extravasation of circulating fluorescently-labelled leukocytes was assessed by using an in vivo videomicroscopy technique. In a second part of the study, the development of vascular damage in short term diabetes was studied in the genetically C6 deficient rats of the PVG strain, and compared with those observed in the wild-type C6 sufficient animals. Here, the analysis of mesentery vascular expression of mRNA for vascular cell adhesion molecule (VCAM)-1, transforming growth factor-β (TGF-β), connective tissue growth factor (CTGF), and platelet-derived growth factor (PDGF), the evaluation of intravascular protein levels of VCAM-1, TGF-β, CTGF, proliferative cell nuclear antigen (PCNA), as well as the assessment of structural changes and Complement components deposition at the mesentery arterial vascular wall were also performed. Conclusions: Leukocyte trafficking, mesentery arteries hypertrophy, extracellular matrix deposition, local vascular gene and protein expression of VCAM-1, TGF-β, CTGF and PCNA, as well as PGDF gene expression were all increased by short term diabetes, but all significantly reduced in the C6 deficient diabetic animals, thus suggesting an active role for TCC in the development of vascular inflammation in the early phases of experimental diabetes.

Original languageEnglish
Pages (from-to)83-89
Number of pages7
JournalAtherosclerosis
Volume216
Issue number1
DOIs
Publication statusPublished - May 2011

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Complement Activation
Innate Immunity
Blood Vessels
Inflammation
Connective Tissue Growth Factor
Mesentery
Vascular Cell Adhesion Molecule-1
Transforming Growth Factors
Complement Membrane Attack Complex
Nuclear Antigens
Leukocytes
Gene Expression
Video Microscopy
Platelet-Derived Growth Factor
Hypertrophy
Extracellular Matrix
Wistar Rats
Proteins
Arteries
Messenger RNA

Keywords

  • Atherosclerosis
  • Diabetes mellitus
  • Inflammation
  • Innate immunity
  • Leukocytes-trafficking
  • Rat
  • Terminal complement complex

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Innate immunity, through late complement components activation, contributes to the development of early vascular inflammation and morphologic alterations in experimental diabetes. / Fischetti, F.; Candido, R.; Toffoli, B.; Durigutto, P.; Bernardi, S.; Carretta, R.; Tedesco, F.; Fabris, B.

In: Atherosclerosis, Vol. 216, No. 1, 05.2011, p. 83-89.

Research output: Contribution to journalArticle

Fischetti, F. ; Candido, R. ; Toffoli, B. ; Durigutto, P. ; Bernardi, S. ; Carretta, R. ; Tedesco, F. ; Fabris, B. / Innate immunity, through late complement components activation, contributes to the development of early vascular inflammation and morphologic alterations in experimental diabetes. In: Atherosclerosis. 2011 ; Vol. 216, No. 1. pp. 83-89.
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AU - Bernardi, S.

AU - Carretta, R.

AU - Tedesco, F.

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